AGE and their receptor RAGE in systemic autoimmune diseases: An inflammation propagating factor contributing to accelerated atherosclerosis

Hans L. A. Nienhuis*, Johanna Westra, Andries J. Smit, Pieter C. Limburg, Cees G. M. Kallenberg, Marc Bijl

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

45 Citations (Scopus)

Abstract

Systemic autoimmune diseases are associated with inflammation, and oxidative stress favouring the formation of advanced glycation endproducts (AGE), able to modulate cellular functions by activation of receptor for advanced glycation endproducts (RAGE). As RAGE expression is increased in an inflammatory milieu, present in patients with systemic autoimmune diseases, these patients are especially prone for the deleterious effects of AGE. Interaction of AGE with RAGE leads to intracellular signalling, and subsequent expression of adhesion molecules, chemokines, pro-inflammatory cytokines and up-regulation of RAGE itself. The AGE-RAGE interaction might act as a pro-inflammatory loop in these patients, contributing to chronic low grade inflammation rendering these individuals susceptible for development of accelerated atherosclerosis.

Original languageEnglish
Pages (from-to)302-304
Number of pages3
JournalAutoimmunity
Volume42
Issue number4
DOIs
Publication statusPublished - 2009

Keywords

  • AGE
  • RAGE
  • inflammation
  • atherosclerosis
  • systemic autoimmune diseases
  • GLYCATION END-PRODUCTS
  • VASCULAR ENDOTHELIAL-CELLS
  • SOLUBLE RECEPTOR
  • PLASMA-LEVELS
  • SERUM-LEVELS
  • ENDPRODUCTS
  • ACTIVATE
  • SRAGE
  • PROTEINS
  • FORM

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